Background: Toxoplasma gondii is a global infection with a crucial role in the development of neurological diseases. Data concerning the association between T. gondii and neurological illnesses in Egyptian children is scarce. Methods: A case-control study was conducted on 60 patients divided into children suffering from central nervous system manifestations without apparent chromosomal anomalies (n=30) and children with Down syndrome (n=30) recruited from Mansoura University Children's Hospital, Mansoura, Egypt. A total of 30 healthy children were included as controls. Demographics and clinical data were collected from all cases and Toxoplasma immunoglobulin (Ig) M and G antibodies were assessed by enzyme-linked immunosorbent assay. Results: Anti-T. gondii IgG was the most frequent antibody detected and the highest seropositivity rates were ranked for the neurologically disabled non-syndromic children, followed by Down syndrome, compared with controls (p <= 0.001). Statistically significant (p=0.05) associations were found between Toxoplasma IgG seropositivity and hydrocephalus and between Toxoplasma IgM and a history of contact with farm animals, soil and cats in children with Down syndrome. Conclusions: The association between Toxoplasma infection and neurological disorders in children should be kept in mind by paediatricians and assessment of T. gondii antibodies in early childhood is needed for timely management of afflicted patients.

Toxoplasma gondii (TG) infection has been reported to be more frequent in schizophrenia. The interaction of the lifelong persisting parasite with the host's immune system involves T-cell/interferon-gamma-induced degradation of tryptophan and provides a challenge to the host well beyond a possible role in the etiology of schizophrenia. The hypothesis we tested in this study was that TG infection may be more frequent (serofrequency) and/or more intense (serointensity) in patients with schizophrenia or major depression compared with psychiatrically healthy controls. In addition, these measures are associated with the clinical course. We did a cross-sectional, prospective investigation of individuals with schizophrenia (n = 277) and major depression (n = 465) admitted to our department (2002-2005) and of healthy controls (n = 214), with all groups adjusted for age and geographic home region. Serofrequency was comparable between the groups, but serointensity was significantly higher in the patients. In individuals with schizophrenia, serointensity was significantly positively associated with C-reactive protein levels and leukocyte counts, and first-episode patients yielded significantly higher serotiters. Immunomodulatory medication was associated with decreased serotiters. In addition, the route of infection appears to differ between patients and controls. Thus, our results support increased host responses to TG infection in the patients, as well as increased titers in first-episode patients with schizophrenia; this may relate to the shifted T-helper 1/2 status described in these patients. Therefore, we suggest that TG infection, particularly in individuals with schizophrenia, is an important environmental factor in the interaction between psychiatric vulnerability, genetic background, immunomodulation, and the neurotransmitter systems.